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The disruption of redox balance in an organism due to oxidative stress typically coincides with the manifestation of disease disorders

The addition of exogenous ROS results in resensitization of cells with high VRK2 expression to GSH inhibition, which is consistent with the fact that PC cells with low expression of VRK2 are susceptible to GSH inhibition attributes to its high basal ROS level, suggesting that cells in a state of oxidative stress have enhanced dependence on the GSH system

This transition between stages II and III after the administration of Vilon was determined to be due to the partial deheterochromatinization-decondensation of the aforementioned fiber loops [2]

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Tiliroside-derivatives enhance GLUT4 translocation via AMPK in muscle cells